abeta42-in-1

β-Amyloid (1-42), acetate (human) is a peptide consisting of 42 amino acids that is part of β-Amyloid and is commonly used in Alzheimer's disease modeling.

Amyloid β Peptide (42-1)(human) acetate is the inactive form of Amyloid β Peptide (1-42). Amyloid β Peptide (42-1)(human) acetate is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease.

Biotin-β-Amyloid (1-42), human TFA, also known as Biotin-Amyloid β-Peptide (1-42) (human) TFA, is a biotin-labeled 42-amino acid peptide implicated in the pathogenesis of Alzheimer's disease.

β-Amyloid (1-42), human, is a 42-amino acid peptide integral to the pathogenesis of Alzheimer disease.

Gastric inhibitory peptide 1 (GIP-1) (3-42), a fragment of the incretin hormone GIP and antagonist to the GIP receptor, is generated through the action of serum dipeptidyl peptidase 4 (DDP-4). When administered at 25 nmol/kg to an ob/ob mouse diabetes model, GIP-1 (3-42) elevates plasma glucose levels and lowers plasma insulin levels, demonstrating its effect on reducing insulin secretion from BRIN-BD11 pancreatic cells at a concentration of 100 nM.

(Nle35)-Amyloid β-Protein (1-42) ammonium is a peptide.

Cys-Gly-Lys-Arg-Amyloid β-Protein (1-42), a peptide fragment derived from amyloid β-protein (Aβ), is crucial in Alzheimer's disease research [1].

FITC-β-Ala-Amyloid β-Protein (1-42) ammonium, a fluorescein isothiocyanate (FITC)-tagged monomer peptide of Aβ1-42, is instrumental in Alzheimer’s disease pathogenesis [1].

(Glu20)-Amyloid β-Protein (1-42) represents a variant of amyloid β-protein (Aβ) that fibrillizes more slowly due to the Glu20 mutation, which diminishes Aβ42's tendency to aggregate and inhibits the accumulation of this slowly fibrillizing peptide. Amyloid β-protein is the principal constituent of amyloid deposits in the vascular system and brain parenchyma in Alzheimer's disease [1] [2].

(D-Asp1)-Amyloid β-Protein (1-42), a peptide fragment of amyloid β-protein (Aβ), serves as the primary constituent of vascular and parenchymal amyloid deposits associated with Alzheimer's disease [1].

(Met(O2)35)-Amyloid β-Protein (1-42) is a peptide [1].

(Met(O)35)-Amyloid β-Protein (1-42) is the oxidized form of Methionine 35 in Aβ42, capable of producing an oligomer size distribution similar to Aβ40. This compound is utilized in Alzheimer’s disease (AD) research [1].

Biotinyl-Ahx-Amyloid β-Protein (1-42) ammonium is an N-terminally biotin-tagged form of Amyloid β-Protein (1-42), the primary component of vascular and parenchymal amyloid deposits associated with Alzheimer's disease [1].

(Gln22)-Amyloid β-Protein (1-42), a Dutch mutation (E22Q) variant of β-Amyloid (1-42), exhibits enhanced fibrillogenic and pathogenic properties [1].

Amyloid (1-42), rat is a polypeptide composed of 42 amino acids. It is toxic to hippocampal slices and can be used in the study of alzheimer's disease.

Piscidin-1 (22-42) is a highly potent, multifunctional Antimicrobial Peptide (AMP) produced by the Orange-spotted grouper (Epinephelus coioides).

Biotinyl-Amyloid β-Protein (1-42) ammonium, a biotinylated form of Amyloid β-Protein (1-42), is used in research on the conversion of Aβ1-42 to Aβ1-40 in the brain [1].

β-Amyloid (1-42), (rat mouse) (TFA), is a 42-amino acid peptide fragment employed in the study of Alzheimer's disease.

[Asn23]-beta-Amyloid (1-42), Iowa mutation, is a biologically active peptide with increased aggregation propensity and fibril toxicity. This mutation involves the substitution of Aspartic acid (Asp) at position 23 with Asparagine (Asn), contributing to autosomal dominant Alzheimer's Disease and associated with severe cerebral amyloid beta-protein angiopathy (CAA) due to a missense alteration at position 694 of the amyloid precursor protein (APP) gene.

'(Asp37)-Amyloid β-Protein (1-42) [1]' refers to the G37D mutant variant of the wild-type Amyloid-beta (1-42) peptide.

β-Amyloid (42-1), human, is the inactive form of Amyloid β Peptide (1-42), which plays a pivotal role in the pathogenesis of Alzheimer's disease.

Gastric inhibitory peptide (GIP) (1-42), an endogenous incretin hormone comprising 42 amino acids, promotes insulin secretion. Expressed in the intestinal neuroendocrine K cells and submandibular gland, it enters circulation after meals. GIP (1-42) blocks histamine, pentagastrin, and insulin-induced gastric acid and pepsin secretion, enhances glucose-stimulated insulin release, and accelerates gastric emptying in rats.

β-Amyloid (1-42), rat TFA is a 42-aa peptide, shows the effects of cytotoxicity on acute hippocampal slices, and has been used in studies of alzheimer's disease.

Piscidin-1 (22-42) (TFA) is a highly potent, multi-functional Antimicrobial Peptide (AMP) produced by Orange-spotted grouper (Epinephelus coioides).

(Gly22)-Amyloid β-Protein (1-42), a peptide fragment of Amyloid β-Protein (Aβ), plays a crucial role in Alzheimer's disease by forming the main component of vascular and parenchymal amyloid deposits. The Glu22 to Gly22 mutation in Aβ is known to enhance aggregation [1] [2].

β-Amyloid (42-1), human TFA, a 42-amino acid peptide, represents the inactive form of Amyloid β Peptide (1-42) and is crucial in the development of Alzheimer's disease [1].

'(Lys22)-Amyloid β-Protein (1-42) represents a mutation of the wild-type (WT) Amyloid β-Protein (1-42) peptide [1].'

[Arg6]-β-Amyloid (1-42), England mutation, is a biologically active peptide linked to autosomal dominant Alzheimer's Disease in various kindreds. The English (H6R) mutation disrupts H6 interactions due to alterations in the beta-amyloid precursor gene.

WRW4 TFA (878557-55-2 free base) is a specific formyl peptide receptor-like 1 (FPRL1) antagonist, inhibits WKYMVm binding to FPRL1 with an IC50 of 0.23 μM. WRW4 TFA(878557-55-2 free base) specifically inhibits the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloid beta42 (Abeta42) peptide, and F peptide.

WRW4 TFA is a formyl peptide receptor-like 1 (FPRL1) antagonist that specifically prevents the binding of WKYMVm to FPRL1 with an inhibition concentration (IC50) of 0.23 μM. It uniquely blocks the rise in intracellular calcium triggered by FPRL1 agonists such as MMK-1, amyloid beta42 (Abeta42) peptide, and F peptide [1].